Assistant Research Professor of Radiation Oncology, Institute for Academic Medicine
Assistant Research Member, Research Institute
Weill Cornell Medical College
Dr. Sengupta is an Assistant Research Member in the department of Radiation Oncology of Houston Methodist Research Institute, and is also affiliated to Houston Methodist Institute for Academic Medicine and Weill Cornell Medical College, New York as Assistant Research Professor. Before joining Houston Methodist in September 2013, he was a Research Scientist at University of Texas Medical Branch at Galveston. He was a 2011-2013 Keck Fellow of Gulf Coast Consortia's Computational Cancer Biology Training Program, funded by the Cancer Prevention and Research Institute of Texas. He received PhD in 2008 from Jadavpur University, India, and is also a recipient of 2007 Young Scientist Award from Indian Institute of Human Genetics. He also serves as a regular reviewer for DNA Repair, Mutation Research, Oncotarget, DNA and Cell Biology, etc.
Dr. Sengupta’s research interest during Ph.D. program was on the defects in DNA mismatch repair genes in the development of microsatellite instability in head and neck squamous cell carcinoma. During his post-doctoral training in Dr. Mitra’s group he worked on transcriptional regulatory aspects of mammalian AP-endonuclease (APE1/Ref-1), an essential DNA base excision repair (BER) protein. Dr. Mitra’s group initially discovered APE1’s N-terminal acetylation (AcAPE1) by histone acetyl transferase p300 at lysines 6 and 7 which modulates its transcriptional regulatory functions. His observations based on promoter ChIP-on-Chip/ChIP-sequencing and global gene Chip expression profile analyses showed APE1/AcAPE1’s involvement in the regulation of diverse set of gene expression in multitudes of pathways associated with tumorigenesis. He elucidated the novel role of APE1 and its acetylation in activating multidrug resistance gene MDR1 that controls tumor cell drug resistance, the repressor role of APE1 in regulation of renin gene that controls blood pressure homeostasis, and the dichotomous regulatory role of APE1 in cell cycle checkpoint gene CDKN1A/p21 regulation by both p53-dependent and independent mechanisms. At present, his interests are to (i) unravel the phenomenon of genome damage and repair during inducible gene activation through reactive oxygen species and (iii) explore BER at the context of chromatin organization particularly on the regulation of repair activities of DNA glycosylase NEIL1 and crosstalk with nucleosome assembly machineries during DNA damage, repair and replication.